ライフサイエンスコーパス: mutant virus

1 ouse studies show extreme attenuation of the mutant virus.

2 ored replication and virulence of the dNSP16 mutant virus.

3 in RAL IC50 than that of the IN-G140S/Q148H mutant virus.

4 s recruited in the airways compared with the mutant virus.

5 ited higher infectivity than either parental mutant virus.

6 the acquisition of transmissibility by this mutant virus.

7 genes) or after infection with the DeltaICP0 mutant virus.

8 tly delayed in cells infected with the pUL25 mutant virus.

9 liver in comparison to those produced by the mutant virus.

10 lial cells following infection with the UL78 mutant virus.

11 emergence of cellular immune response to the mutant virus.

12 d in comparison to those inoculated with the mutant virus.

13 sm comparable to the known phenotype of UL32 mutant virus.

14 A blocked apoptosis induced by a Deltaalpha4 mutant virus.

15 was not able to complement the Ad5 L1-52/55K mutant virus.

16 llowed faster and higher-titer production of mutant virus.

17 HA) mRNA nuclear export was seen with an NS1 mutant virus.

18 but not CLDN1, were infectable only with the mutant virus.

19 nd the infectivity of a class II IN deletion mutant virus.

20 genetically engineered CTL epitope-deficient mutant virus.

21 RNA in virions of wild-type, but not escape mutant, virus.

22 athology following intranasal infection with mutant viruses.

23 multiple mutations were less fit than single-mutant viruses.

24 d in cells infected with wild-type and ORF12 mutant viruses.

25 from mice infected with wild-type or glycan mutant viruses.

26 e characteristics were unchanged for the two mutant viruses.

27 high titers of neutralizing activity to the mutant viruses.

28 HTLV-2 infection in vivo, we generated APH-2 mutant viruses.

29 carbohydrate and JAM-A by the length and IDR mutant viruses.

30 ented the replication of A8 and A23 deletion mutant viruses.

31 y to evaluate the antigenic phenotype of the mutant viruses.

32 a dominant-negative, deacetylase-dead point mutant virus (AAV-HDAC3(Y298H)-v5), we found that select

33 cytokines, whereas the vhs deletion (vhs(-)) mutant virus activated DCs without the need for exogenou

34 Thus, this mutant virus adapted to the loss of CLDN1 by developing

35 reated or IFN-treated cells infected by this mutant virus (AdEasyE1Sub19) contained much higher stead

36 Finally, we created a second UL79 mutant virus (ADinUL79(stop)) in which the UL79 ORF was

37 we engineered a recombinant KSHV ORF52-null mutant virus and found that loss of ORF52 results in red

38 Using reverse genetics, we engineered Ubl mutant viruses and found that AM2 (V787S) and AM3 (V785S

39 We constructed the corresponding pol mutant viruses and found that the polDeltaN43 mutant dis

40 g rates of wild-type virus, fitness costs of mutant virus, and growth rates of both viruses.

41 Since wt virions could not complement the mutant viruses, and the mutant viruses did not effective

42 and most viral gene expression of the L4-33K mutant virus are comparable to those of the wild-type vi

43 We find that E99V mutant viruses are defective for fusion with cell membra

44 e not required for effective host control of mutant virus as all N1347A virus-infected mice survived

45 Ultrasensitive quantification of the mutant viruses at the early developmental stage is even

46 eceptor homolog, with the infectivity of one mutant virus being >500-fold less with the quail TVA rec

47 ffectively attenuated the resulting SARS-CoV mutant viruses both in vitro and in vivo.

48 nt the plaque-forming defect of an ICP0-null mutant virus but also to mediate the derepression of qui

49 of PACT compromised IFN-I activation by the mutant virus, but not wild-type virus, a finding consist

50 ile in IFN-deficient Vero cells, both WT and mutant viruses can replicate at relatively high levels.

51 re explained in part by the observation that mutant viruses carrying NNRTI plus INSTI resistance muta

52 Characterization of mutant viruses carrying phenylalanine (Phe)-to-alanine (

53 ated from lesions of animals inoculated with mutant virus contained mutations in the area of 3A that

54 The mutant viruses contained mutations in the hr1 region of

55 The mutant virus containing a substitution of Ala for Arg in

56 An LR mutant virus containing stop codons at the amino terminu

57 ing the latency-reactivation cycle because a mutant virus containing stop codons at the amino terminu

58 tal virus, SAT2/ZIM/7/83, indicated that the mutant virus containing the TQQS-to-ETPV mutation in the

59 In vitro susceptibility measurements with mutant viruses containing amino acid substitutions K70G,

60 infection of JCPyV by generating a panel of mutant viruses containing amino acid substitutions of th

61 ortant for these cellular processes and that mutant viruses containing mutations of CrPV-1A attenuate

62 owth of a B1-deficient temperature-sensitive mutant virus (Cts2 virus) in U2OS osteosarcoma cells.

63 hree antibodies had neutralizing activity to mutant viruses deficient in gp41 carbohydrate attachment

64 y using two viruses null for IVa2-a deletion mutant virus, DeltaIVa2, and the previously described mu

65 of IFN-alpha/betaR-/- mice with the G50DblKo mutant virus demonstrated partial rescue of (i) acute vi

66 that recombinant E119D and E119A/D/G/-H274Y mutant viruses demonstrated reduced inhibition by all of

67 s; further, the recombinant T205-substituted mutant viruses described here would appear to be the fir

68 nduced by infection with an E1B 19K deletion mutant virus did not repress macrophage proinflammatory

69 d not complement the mutant viruses, and the mutant viruses did not effectively inhibit wt gene expre

70 Here we describe the creation of mutant viruses directly in the multicellular organism C.

71 ntly, compared with the wild-type virus, the mutant virus displayed a decreased capacity to infect an

72 In addition, these mutant viruses displayed an infection defect in monkey c

73 However, the drift mutant viruses displayed reduced stability, and we predi

74 All cleavage-site mutant viruses displayed reduced thermostability, with d

75 port that inoculation of swine with this SAP-mutant virus does not cause clinical signs of disease, v

76 re, we show that pro-necrotic murine CMV M45 mutant virus drives virus-induced necroptosis during non

77 Viral growth of mutant virus encoding K229R, mimicking a non-acetylated

78 everely impaired compared to wildtype or the mutant viruses encoding K77R or K113R.

79 The HSV-1(F) gBDelta28syn mutant virus, encoding a carboxyl-terminal truncated gB,

80 TB reaction pharmacologically or by using a mutant virus enhanced or inhibited transmission, respect

81 In vitro, mutant viruses entered fibroblasts and epithelial cells

82 ere, we demonstrate that in U2OS cells, a B1 mutant virus escapes the block in DNA replication observ

83 its inoculated with either wtHTLV-2 or APH-2 mutant viruses established a persistent infection.

84 In contrast, the mutant virus EV11-207R is not transferred to tight junct

85 When transmitted, the mutant virus eventually reverted to the wild type in 2 o

86 This mutant virus exhibited a delayed disease in cattle compa

87 In vivo, the NLR nonbinding F1L mutant virus exhibited an attenuated phenotype similar t

88 The mutant virus exhibited drastically reduced expression of

89 rus-infected controls, animals infected with mutant virus exhibited higher viral load in cerebrospina

90 Correspondingly, the ORF64 DUB active site mutant virus exhibited impaired ability to establish lat

91 The mutant virus exhibited two functional alterations as com

92 wer-fidelity W237I (W237I(LF)) and W237L(LF) mutant viruses exhibited lower ribavirin resistance.

93 These mutant viruses exhibited normal capsid morphology but we

94 erved in other cell types and, instead, this mutant virus exhibits impaired late protein accumulation

95 The DC480 mutant virus expressed full-size UL37 as detected by the

96 ble to produce infectious virus in DCs, this mutant virus expresses early and late genes.

97 A mutant virus expressing NCp15 shows greatly reduced infe

98 s or in the livers of infected mice, whereas mutant viruses expressing inactive VP3-CTD (H718A or H79

99 However, unlike the wild-type virus, the mutant virus failed to enter into the axoplasm of gangli

100 Experimental infections with mutant viruses generated by using reverse genetics indic

101 l, comparisons of single, double, and triple mutant viruses generated in the same HSV-1(F) genetic ba

102 Indeed, mutant virus genomes deficient for IE1 expression exhibi

103 The mutant virus gK-V5-TEV was subsequently constructed by i

104 In vaccinated animals, the GP85 mutant virus (GP85 DISC) induced an antibody response to

105 in human skin xenografts, while the YY1 site mutant virus grew as well as the wild type in MeWo cells

106 In both cell culture and mosquitoes, the mutant viruses grew equivalently and did not revert to w

107 The HA-K582I mutant virus had greater growth and virulence in DBA/2J

108 In vitro, the mutant virus had reduced binding and infectivity in chol

109 Likewise, the RT-E138K plus IN-G140S/Q148H mutant virus had significantly greater fold increases in

110 S/Q148H and the RT-E138K plus IN-G140S/Q148H mutant viruses had significantly greater fold increases

111 It reveals that the transmissible-mutant virus has a 200-fold preference for binding human

112 he PICV Z protein, although producing viable mutant viruses, have significantly reduced virus growth,

113 ximately 51-nucleotide contiguous subsegment mutant viruses having synonymous mutations revealed that

114 failed to support the replication of an ICP8 mutant virus in a complementation assay.

115 to complement the growth of an Ad5 L1-52/55K mutant virus in conjunction with the Ad17 structural pro

116 Consequently, the ratio of mutant virus in feces is reduced following additional cy

117 The same mutant virus in mice also enhanced virus replication and

118 s improved the fitness of the IN-G140S/Q148H mutant virus in the presence of raltegravir (RAL); the R

119 support spread of progeny virus was an HAdV3 mutant virus in which formation of PtDd was disabled (mu

120 We created a mutant virus in which sequences encoding these residues

121 that prevent reproduction and spread of the mutant viruses in human cells.

122 hout infection with either wild-type or ICP0 mutant viruses in human embryonic lung cells (HEL) or HE

123 n of viral siRNAs and rapid clearance of the mutant viruses in mice.

124 assessed the stability of the 18 recombinant mutant viruses in regard to their growth kinetics, antig

125 n gene expression elicited by the native and mutant viruses in the lungs of infected mice were determ

126 Here, we constructed specific mutant viruses in which translation of D10 was prevented

127 Thus, the mutant virus incurs a fitness cost when environmental st

128 icated that the NV-deficient and NV knockout mutant viruses induce apoptosis earlier in cell culture

129 The LR mutant virus induces higher levels of apoptotic neurons

130 However, E1B-55K mutant virus-infected cells became trapped in a mitotic-

131 were observed in the extracellular space in mutant virus-infected cells in the presence or absence o

132 the nucleus is severely compromised in UL92 mutant virus-infected cells, and mature virions are not

133 istribution in UL96, UL32, or UL96/UL32 dual mutant virus-infected cells.

134 reconstituted by plasmid transfection and in mutant virus-infected cells.

135 n the wild-type virus-infected cells and the mutant virus-infected cells.

136 Immunofluorescence imaging of nsp15 mutant virus-infected macrophages revealed significant d

137 ages is dramatically increased during double-mutant virus infection and correlates with faster antivi

138 f UV treatment, lentivirus transduction, and mutant virus infection experiments, our results demonstr

139 ld-type virus, while polDeltaN52 and polA(6) mutant virus infection resulted in an 8-fold defect in v

140 ired to attenuate disease following PP1alpha-mutant virus infection.

141 Remarkably, SAP-mutant virus-inoculated animals developed a strong neutr

142 mpairs HIV infectivity and that the protease mutant virus is arrested during the early postentry stag

143 onstrate that the phenotype of an Ad5 L4-33K mutant virus is complex.

144 mice with WT or AM2 virus and found that the mutant virus is highly attenuated, yet it replicates suf

145 Although the mutant virus is no longer able to propagate by extracell

146 Here we show that replication of ns2 mutant viruses is attenuated in bone marrow-derived macr

147 can partially complement a growth-defective mutant virus lacking both UL21a and UL97, with significa

148 A mutant virus lacking the mu2 ITAM activates NF-kappaB le

149 Mutant viruses lacking hydrolase activity were unable to

150 Mutant viruses lacking this gene product exhibit dramati

151 deletions in the CT, we were able to rescue mutant viruses lacking two or four residues (rDelta2 and

152 3 inhibitor, GSK872, and infection with this mutant virus led to phosphorylation and aggregation of M

153 restore infectivity to maturation-defective mutant viruses led us to hypothesize that SP may play an

154 Mutant viruses locked in either state remain competent t

155 Additionally, most of the mutant viruses lost the capacity to escape MxA restricti

156 Surprisingly, the A77V mutant virus maintained the ability to replicate in mono

157 dilated cardiomyopathy, suggesting that such mutant viruses may be the forms responsible for persiste

158 Quantification of the mutant viruses may help in predicting the risk of HCC.

159 asmid (McKbac) and utilized to construct the mutant virus McK(gKDelta31-68), carrying a 37-amino-acid

160 terferon production in the host but rendered mutant viruses more susceptible to interferon compared t

161 of mice with the macrodomain catalytic point mutant virus (N1347A) resulted in reductions in lethalit

162 Two capsid missense mutant viruses, N74D and P90A, were largely insensitive

163 A mutant virus, named Ban/AF, was developed in which the v

164 iii) that in cells infected with a DeltaICP0 mutant virus, Nectin-1 remained on the cell surface.

165 miRNA mutant viruses of some members of the Polyomaviridae exp

166 -KO Huh-7.5 cells supported infection by the mutant virus only when CLDN1, CLDN6, or CLDN9 was expres

167 The defects in assembly of gE(-) US9(-) mutant virus particles were novel because they were neur

168 Late-domain mutant virus particles were seen at the uropod in form o

169 In all cases, the mutant virus particles, as well as the antibody-bound wi

170 In vivo, both WT and F1/F2 mutant viruses persistently infected mice, although F1,

171 Analysis of the mutant virus phenotype indicates that accumulation of ca

172 C terminus of the V gene in PIV5 results in mutant viruses (PIV5DeltaSH and PIV5VDeltaC) that enhanc

173 rus, DeltaIVa2, and the previously described mutant virus, pm8002.

174 However, in cells infected with this mutant virus, PML formed novel track-like structures tha

175 protect mice against lethal challenge of the mutant viruses, possibly owing to its ability to mediate

176 veolar lavage fluid after infection with the mutant virus PR8 A/NS1-Y89F (PR8 Y89F) when compared wit

177 ar clone JFH-1, thereby producing a range of mutant viruses predicted to possess altered RNA secondar

178 Although the DeltaUS17 mutant virus produced numbers of infectious particles in

179 These mutant viruses produced smaller foci of infection in Ver

180 The L4-33K mutant virus produces only empty capsids, indicating a d

181 ing of this mutant confirmed the presence of mutant virus protein in the transfected BHK cell lysate.

182 Of the 14 single and double mutant viruses recovered in the backbone of pH1N1, four

183 he -3 position was found to be important for mutant virus recovery.

184 The mutant viruses remained susceptible to favipiravir.

185 The mutant viruses replicate poorly in the brains of infecte

186 The mutant virus replicated similarly to the wild type in vi

187 npermissive for VACV; however, wild-type and mutant viruses replicated in triple-KO cells in which RN

188 Although parental and mutant viruses replicated somewhat better in ducks than

189 d lead directly to its discovery by rescuing mutant virus replication in nonactivated T cells.

190 The efficiency of mutant virus replication was similar to that of wild-typ

191 ma1 IDRs to generate DeltaIDR1 and DeltaIDR2 mutant viruses, respectively.

192 Infection with the mutant virus resulted in a significant decrease in viral

193 Interestingly, the mutant virus retained partial PF74 binding, and its repl

194 Sequencing revealed that the mutant virus retained the original cytoplasmic tail dele

195 Further characterization of the mutant viruses revealed differences in particle morpholo

196 Analysis of revertant SL-1 mutant viruses revealed that a compensatory mutation in

197 isolate with a US17 deletion (the DeltaUS17 mutant virus) revealed blunted host innate and interfero

198 context of cells infected with wild-type or mutant virus, reversing the charge of these two residues

199 However, in the majority of the animals, the mutant virus reverted back to the wild-type sequence, he

200 Strikingly, glyco-Gag mutant virus reverted to glyco-Gag-containing virus only

201 ately twice as many upregulated genes in the mutant virus samples by 48 h postinfection, despite iden

202 dicating that cells infected with a UL97-L1m mutant virus show no defects in growth or E2F-responsive

203 to the wild-type virus, the ToV-PLP knockout mutant virus showed impaired growth and induced higher e

204 restingly, in mice the neutralization escape mutant viruses showed either attenuation (Urbani backgro

205 Upon infection of guinea pigs, the RNase mutant viruses stimulate strong IFN responses, fail to r

206 The recombinant A/Puerto Rico/8/34 (rPR8) mutant virus strain was attenuated and caused reduced mo

207 uation to generate W7-791, a live attenuated mutant virus strain.

208 , and RFC5 mRNAs also enhanced spread of the mutant virus, strengthening the biological significance

209 , amantadine and rimantadine, while the S31N mutant viruses, such as the pandemic 2009 H1N1 (H1N1pdm0

210 ters in the brains of mice infected with the mutant virus suggest that the alphavirus TF protein is i

211 escued the virulence of the PP1alpha-binding mutant virus, suggesting an IFN-independent role for eIF

212 lls infected with a newly isolated UL32-null mutant virus, suggesting that UL32 acts as a chaperone c

213 le in cells infected with E1B-55K or E4-ORF6 mutant viruses, suggesting that Ad regulates paralog-spe

214 teraction did not affect the HA titer of the mutant viruses, suggesting that the same amount of viral

215 of the wild-type virus with all the p24(CA) mutant viruses tested.

216 We recently described a mutant virus that bypasses the requirement for cell surf

217 he latency-reactivation cycle, because an LR mutant virus that contains three stop codons downstream

218 We developed a FMDV mutant virus that could not bind DCTN3.

219 y as the wild-type virus; however, the smD1' mutant virus that does not express NS2 and NS4 underwent

220 Importantly, the smA1' mutant virus that does not express NS3 and NS4 replicate

221 ine expressing A30.5, we isolated a deletion mutant virus that exhibits a defect in morphogenesis in

222 Intriguingly, a TAg mutant virus that is unable to activate the DDR causes s

223 When exposed to CD11(+) DCs, the mutant virus that lacks the amino terminus of gamma134.5

224 Although the G147R NA receptor-binding mutant virus that we characterize is a laboratory creati

225 Using mutant viruses that are defective for nuclear entry, we

226 1, and 508 to 518) have been identified, and mutant viruses that block phosphorylation sites within e

227 We analyze a panel of mutant viruses that contain different amino acid substit

228 become functionally exhausted or select for mutant viruses that escape T cell recognition.

229 proportion of individuals remain infected by mutant viruses that escape the vaccine.

230 In addition, we found that mutant viruses that express an unstable form of the UL10

231 mutant, wild-type, and HA-H241Q and HA-K582I mutant viruses that have HA activation pH values of 6.3,

232 We created mutant viruses that incorporate most of the approximatel

233 s, we attempted the recovery of a panel of V mutant viruses that individually contained one of six cy

234 Growth analyses of mutant viruses that lack each individual miRNA revealed

235 of action of these inhibitors, we generated mutant viruses that were resistant to the inhibitory eff

236 o AD-5 and neutralization activity toward gB mutant viruses that were similar to those of AD-5-specif

237 To address this, we generated UL69 mutant viruses that were unable to interact with SPT6 an

238 However, DC480 mutant virus titers increased nearly 20-fold when the vi

239 increases neutralization sensitivity of the mutant virus to CD4 binding site (CD4bs)-directed antibo

240 We generated and characterized an Ad5 L4-33K mutant virus to further explore its function(s) during i

241 Additionally, the inability of the mutant viruses to efficiently inhibit host protein synth

242 dergo continual antigenic evolution allowing mutant viruses to evade host immunity acquired to previo

243 We generated and characterized two L4-22K mutant viruses to further explore L4-22K functions durin

244 MDC-mediated capture and transmission of MA mutant viruses to T cells were decreased, suggesting tha

245 with normal kinetics in cells infected with mutant virus, UL103 appears to function during the late

246 Here, we characterize a UL93 stop mutant virus (UL93st-TB40/E-BAC) to demonstrate that the

247 These findings may explain why ORF75c mutant viruses unable to degrade PML had no demonstrable

248 MHV68 G50DblKo virus demonstrated that this mutant virus was able to establish latency in the spleen

249 AR1-sufficient CON(kd) cells, only the C(ko) mutant virus was an effective inducer and the IFN-beta R

250 A conditional lethal mutant virus was constructed by placing the A19 open rea

251 The mutant virus was debilitated in primary T cells and macr

252 DV1 was lethal, since no replication of the mutant virus was detected in human cells.

253 When the UL92 mutant virus was evaluated, function was fully complemen

254 nce of EFV, the RT-E138K plus IN-G140S/Q148H mutant virus was fitter than one with the RT-E138K mutat

255 2J mice than the wild type did, although the mutant virus was highly attenuated in ducks.

256 The HA-Y231H mutant virus was highly susceptible to acid inactivation

257 Moreover, the replication of the mutant virus was markedly impaired in activated primary

258 The higher-fidelity W237F (W237F(HF)) mutant virus was more resistant to the mutagenic nucleos

259 ependent on the viral protein NSs, as an NSs mutant virus was not found to induce the equivalent sign

260 An ns2 mutant virus was unable to replicate in the liver or ind

261 ingle-cycle (DISC) vaccine strategy, a GPCMV mutant virus was used that lacked the ability to express

262 at the membrane fusion step, and while this mutant virus was viable, it was significantly attenuated

263 n cytoplasmic virion envelopment, a cadre of mutant viruses was constructed and characterized.

264 istance mutations on the fitness of RT-Y181C mutant viruses was observed.

265 the replication of the S224A and S224A/T226A mutant viruses was reduced in cell culture and in vivo.

266 The phenotype of many of these mutant viruses was the accumulation of large open capsid

267 Using a miR-H2-deficient mutant virus, we found no evidence that miR-H2 represses

268 By studying A6 mutant viruses, we found that A6 plays an essential role

269 verity and lethality caused by the different mutant viruses, we have identified specific residues loc

270 ncing of cyclophilin A (CypA), as well as CA mutant viruses, we implicated CypA in the SUN2-imposed b

271 Levels of mutant virus were dramatically reduced upon amplificatio

272 rse transcription reactions of the glyco-Gag mutant virus were substantially inhibited compared with

273 on of viral genes, the plaques formed by the mutant virus were very small, implying a defect in virus

274 No differences between the WT and DeltaNA mutant viruses were detected with respect to effects on

275 of the F proteins expressed by the recovered mutant viruses were efficiently cleaved and transported

276 The resulting mutant viruses were evaluated in tissue culture and in m

277 While the UL15, UL32, and UL54 mutant viruses were fully susceptible to raltegravir, an

278 In the present study, 10 mutant viruses were generated to determine which residue

279 res, the immortalization capacities of APH-2 mutant viruses were indistinguishable from that of wild-

280 In the absence of drug, single-mutant viruses were less fit than the wild type; viruses

281 24)LL3D(YR) and double A(24)LL3B(PVKV)3D(YR) mutant viruses were markedly attenuated upon inoculation

282 Differences between wild-type and sigma1 mutant viruses were not attributable to alterations in s

283 tly infected mice, although F1, F2 and F1/F2 mutant viruses were rapidly eliminated 1-7 days post-ino

284 Both mutant viruses were significantly less dependent on SR-B

285 Instead, these mutant viruses were unable to expose VP2 upon arrival to

286 address this question, we took advantage of mutant viruses whose viral entry into cells relies on th

287 A mutant virus with deletion of NS1 induced high levels of

288 An LR mutant virus with stop codons at the amino terminus of O

289 An LR mutant virus with stop codons at the amino terminus of t

290 An LR mutant virus with stop codons at the amino terminus of t

291 Mutant viruses with increased frameshift efficiencies ha

292 We demonstrated that mutant viruses with RBS deletions are able to escape pol

293 Competitive growth of the escape mutant viruses with the wild-type virus revealed that so

294 h specificity for SAalpha2,3 and the other a mutant virus (with Q226L and G228S in the HA) with prefe

295 calized in nuclei of cells infected with the mutant virus, with fewer cytoplasmic capsids detected.

296 in the viral polymerase (L protein) of most mutant viruses, with the vast majority of the amino acid

297 e the wild-type virus, it can also bind to a mutant virus without inhibiting fusion or attachment.

298 Surprisingly, ICP0-null mutant virus yields decreased upon TRIM27 depletion, arg

299 Mutant virus yields from multiple-round infections were

300 (ZEBOV), mouse-adapted virus (MA-ZEBOV), and mutant viruses (ZEBOV-NP(ma), ZEBOV-VP24(ma), and ZEBOV-